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1.
New Emirates Medical Journal ; 3(2), 2022.
Article in English | Scopus | ID: covidwho-2270747

ABSTRACT

Background: Fetal neurons are sensitive to ischemia which could happen secondary to acute maternal blood loss. The damage to the fetal brain with loss of braineurons in early gestation leads to encephalomalacia. We describe here a case report of fetal encephalomalacia secondary to acute maternal blooloss. Case Presentation: A 23-year-old gravida 3, para 2 woman sustained a forearm laceration at 18 weeks of gestation. Her hemoglobin dropped to 7.9 mg/dL. A surgicalaceration repair was completed, and she was transfused with blood. At the OB visit the following week, her fetal US showed abnormal brainevident by the increased size of the lateral ventricles. A follow-up MRI at 30 weeks of gestation confirmed fetal encephalomalacia. A completinvestigation, including free cell maternal DNA for chromosomal anomalies, TORCH infection, and Covid PCR, all were negative. Conclusion: We concluded from the case that any history of significant acute maternal blood loss that required blood transfusion should necessitate a fetaultrasound to look for fetal well-being, especially for any brain structural changes in the developing brain. © 2022 Shabih Manzar et al.

2.
Neurology ; 98(18 SUPPL), 2022.
Article in English | EMBASE | ID: covidwho-1925354

ABSTRACT

Objective: Stroke has been reported to be a potential neurological complication of COVID-19 infection in adults, however, only a few reports have been made in the pediatric population. We describe a case of a 12-year-old female with post-COVID-19 syndrome who was found to have an ischemic stroke on MRI as well as positive for lupus anticoagulant. Background: COVID-19 has been documented to potentiate a prothrombotic and proinflammatory state. It is postulated this occurs via endothelial cell disruption and clotting cascade activation. However, cases have reported the presence of prothrombotic antibodies in patients with COVID-19 infections. The persistent presence of these antibodies has important clinical implications, including an increased thrombotic risk. Design/Methods: Chart review Results: A 12-year-old female with history of migraines presented to the neurology clinic for increased frequency and severity of headaches. Patient reported to have COVID-19 infection one year prior with symptoms of fatigue, arthralgias, sore throat, and headaches. Following infection, patient had resolution of most symptoms but continued having increased headaches and difficulty concentrating. Headaches have been occurring multiple times per week, lasting hours to days, and are associated with nausea, vomiting, and photophobia. Patient has no focal neurological deficits. Brain MRI showed small focal encephalomalacia with surrounding gliosis and volume loss in the anterior right basal ganglia and adjacent external capsule consistent with a small chronic infarct. On thrombophilia work-up patient was positive for lupus anticoagulant and had a heterozygous MTHFR variant. Patient was started on baby aspirin and her headaches have been controlled with prophylactic co-enzyme Q-10 and naproxen. Conclusions: Due to the known prothrombotic risk of COVID-19 infections, there should be a high index of suspicion for stroke symptoms among pediatric patients with COVID-19. Improved clinical surveillance and increased screening for prothrombotic antibodies could ensure better outcomes, including timely treatment and prevention of complications.

3.
Brain Dev ; 44(10): 743-747, 2022 Nov.
Article in English | MEDLINE | ID: covidwho-1926245

ABSTRACT

INTRODUCTION: The coronavirus disease 2019 (COVID-19), including the Omicron variant, is less severe in children than in adults. To date, there has been no detailed description of COVID-19-associated severe encephalopathy due to the Omicron variant during the neonatal and early infantile periods. CASE PRESENTATION: During the outbreak of the Omicron variant, a 29-day-old male presented with a pale and ill appearance. The patient was intubated for mechanical ventilation owing to recurrent apnea, which subsequently turned out to be a breath-holding that may have been caused by seizure. In addition, nonconvulsive status epilepticus was observed. Total duration of repetitive seizure activities was approximately 30 min per hour when seizures were most severe. Brain magnetic resonance imaging (MRI) on day 14 revealed extensive hyperintensity in the T2 sequence, hypointensity in the fluid-attenuated inversion recovery (FLAIR) sequence in the deep and subcortical white matter, and diffusion restriction in the corpus callosum. The Omicron BA.1 variant of the severe acute respiratory syndrome coronavirus 2 was detected in his respiratory sample. Follow-up MRI on day 45 revealed multiple cystic cavitations. CONCLUSION: Although COVID-19 is not severe in most children, life-threatening conditions such as COVID-19-associated severe encephalopathy can occur during the neonatal and early infantile periods.


Subject(s)
Brain Diseases , COVID-19 , Infant, Newborn , Adult , Child , Humans , Male , COVID-19/complications , SARS-CoV-2 , Brain Diseases/etiology , Brain Diseases/complications , Seizures/etiology
4.
Journal of Investigative Medicine ; 70(2):466-467, 2022.
Article in English | EMBASE | ID: covidwho-1706950

ABSTRACT

Case Report Disseminated Herpes Simplex Virus (HSV) is a feared neonatal infection typically presenting after the first week of life with sepsis-like features and encephalopathy. Congenitally acquired HSV infection represents a rare, serious variety of HSV in the neonatal period, providing a unique diagnostic challenge with significant morbidity and mortality. A female infant was delivered at 29.2 weeks gestational age via cesarean section in the setting of non-reassuring fetal heart tracings, maternal preeclampsia, gestational diabetes, and Sars- COV2 infection. Physical exam at 1 hour of life demonstrated erosive lesions of the knee, foot, and cheek. Dermatology was consulted and favored infectious source of lesions, so a sepsis evaluation including HSV, VZV, and CMV studies was performed and ampicillin, gentamicin, acyclovir, and amphotericin B were started. Given high concern for HSV vs. varicella, ophthalmology was consulted, finding bilateral, likely viral, retinitis. Laboratory evaluation revealed transaminitis, thrombocytosis, and CSF pleocytosis with elevated protein. HSV PCR was positive in blood, CSF, and cutaneous lesion, as well as HSV2 positive on surface culture, yielding the diagnosis of congenital disseminated HSV with meningoencephalitis. The remainder of infectious studies were negative. There was no known maternal HSV history, although placental pathology revealed positive immunohistochemical staining for HSV 1/2 in addition to Sars-COV2. Patient's serial CSF and blood HSV remained positive despite treatment with acyclovir. Serial HUS showed initially normal findings that progressively worsened to feature bihemispheric cystic encephalomalacia, periventricular leukomalacia with ex vacuo dilation of lateral and third ventricles. She developed central diabetes insipidus and was started on desmopressin. Ocular involvement subsequently included retinal necrosis and diffuse retinal hemorrhage. She developed severe myoclonic jerks in the absence of electrographic correlate on EEG. Levetiracetam and phenobarbital alleviated jerks, although she developed progressive hypotonia as neurologic status continued to deteriorate. Considering persistently positive HSV studies, foscarnet was added to acyclovir. However, at 3 weeks of life, she was intubated for apnea and respiratory failure, and given clinical trajectory and devastating prognosis, mother asked to compassionately withdraw support and allow natural death on day of life 25. This case of congenital, disseminated HSV is particularly unique in that it occurred in a premature infant of 29 weeks gestation and had significantly elevated copy numbers in the blood and CSF as well as skin lesions, indicating likely longstanding infection at the time of delivery. Additionally, it is unknown how concurrent placental viral infections with SARSCoV2 may have contributed to this patient's course, or if the recent maternal SARS-CoV2 infection may triggered HSV reactivation and subsequent congenital HSV.

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